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Clinical diagnostic value and potential regulatory mechanisms of lncRNA NOP14-AS1 in chronic kidney disease.
Nucleosides Nucleotides Nucleic Acids
January 2025
Urology & Nephrology Center, Department of Nephrology, Zhejiang Provincial People's Hospital (Affiliated People's Hospital), Hangzhou Medical College, Hangzhou, China.
In the early stages, chronic kidney disease (CKD) can be asymptomatic, marking diagnosis difficult. This study aimed to investigate the diagnostic role and potential regulatory mechanisms of nucleolar protein 14 (NOP14) -antisense RNA 1 (AS1) in patients with CKD. Herein, 68 patients with CKD, 65 patients with CKD undergoing peridialysis, and 80 healthy adults were included.
View Article and Find Full Text PDFSivelestat sodium protects against renal ischemia/reperfusion injury by reduction of NETs formation.
Arch Biochem Biophys
January 2025
Department of Critical Care Medicine, the First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang Province 150001, China; Heilongjiang Provincial Key Laboratory of Critical Care Medicine, Harbin 150001, China; Central Laboratory of The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang Province, China. Electronic address:
Background: Ischemia-reperfusion injury (IRI) often results in renal impairment. While the presence of neutrophil extracellular traps (NETs) is consistently observed, their specific impact on IRI is not yet defined. Sivelestat sodium, an inhibitor of neutrophil elastase which is crucial for NET formation, may offer a therapeutic approach to renal IRI, warranting further research.
View Article and Find Full Text PDFLong-lived cytokinetic bridges coordinate sister-cell elimination in mouse embryos.
Dev Cell
January 2025
Centre de recherche du Centre Hospitalier de I'Université de Montréal (CRCHUM), Montréal, QC H2X 0A9, Canada; Department of Obstetrics and Gynaecology, and Department of Pathology and Cell Biology, Université de Montréal, Montréal, QC H3T 1C5, Canada. Electronic address:
Apoptosis is a key feature of preimplantation development, but whether it occurs in a cell-autonomous or coordinated manner was unknown. Here, we report that plasma membrane abscission, the final step of cell division, is profoundly delayed in early mouse embryos such that a cytokinetic bridge is maintained for the vast majority of the following interphase. Early embryos thus consist of many pairs of sister cells connected by stable cytokinetic bridges that allow them to share diffusible molecules.
View Article and Find Full Text PDFUtero-placental adaptations in response to intrauterine growth restriction in swine.
Domest Anim Endocrinol
January 2025
Department of Animal Science, Pennsylvania State University, University Park, PA, 16802, USA. Electronic address:
Intrauterine growth restriction (IUGR) is a common condition in swine associated with high piglet mortality and morbidity that develops in early gestation. This review article explores differences in uterine and placental tissues associated with IUGR fetuses compared to their normally-grown littermates at different stages of gestation. Specifically, we will review the available knowledge to date describing differences in 1) structure, 2) cellular apoptosis and proliferation, 3) adhesion, and 4) angiogenesis in endometrial and placental tissues associated with IUGR fetuses across gestation.
View Article and Find Full Text PDFThe Hao-Fountain syndrome protein USP7 regulates neuronal connectivity in the brain via a novel p53-independent ubiquitin signaling pathway.
Cell Rep
January 2025
Department of Neurological Surgery, Washington University School of Medicine, St. Louis, MO 63110, USA; Department of Neurology, Washington University School of Medicine, St. Louis, MO 63110, USA; Department of Genetics, Washington University School of Medicine, St. Louis, MO 63110, USA; The Brain Tumor Center, Siteman Cancer Center, Washington University School of Medicine, St. Louis, MO 63110, USA. Electronic address:
Mutation or deletion of the deubiquitinase USP7 causes Hao-Fountain syndrome (HAFOUS), which is characterized by speech delay, intellectual disability, and aggressive behavior and highlights important unknown roles of USP7 in the nervous system. Here, we conditionally delete USP7 in glutamatergic neurons in the mouse forebrain, triggering disease-relevant phenotypes, including sensorimotor deficits, impaired cognition, and aggressive behavior. Although USP7 deletion induces p53-dependent neuronal apoptosis, most behavioral abnormalities in USP7 conditional knockout mice persist following p53 loss.
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